Neurohypophysial disorders Flashcards

1
Q

How does the PPg appear in MRIs?

A

A bright spot- always use MRIs to visualise pituitary gland

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2
Q

What hormones come from the PPG?

A

Oxytocin

Vasopressin (ADH)

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3
Q

APG and PPG types of tissue

A

APG- glandular tissue

PPG- neural tissue

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4
Q

How does vasopressin act?

A

Vasopressin is an antidieuretic. It acts to increase water reabsorption from renal cortical and medullary collecting ducts (via V2 receptors).

When vasopressin binds to the V2 receptor of the collecting duct cell, it acts so that AQP2 aquaporins are inserted to the lumen side (apical) of the membrane. There is increased water uptake into the cell and therefore into the plasma (through V3 and V4 receptors).

Water travels in across osmotic gradient and the net result is water reabsorption.

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5
Q

What regulates vasopressin release

A

Osmoreceptors

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6
Q

Where are the osmoreceptors located?

A

Organum vasculosum (near the hypothalamus)

They project through the supraoptic nucleus and the paraventricular nucleus.

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7
Q

How do the osmoreceptors chnage in shape?

A

Osmoreceptors are really sensitive to changes in extracellular osmolality. An increase in extracellular Na+ increases the osmolality of the surrounding extracellular environment. Water leaves the osmoreceptors, down the concentration gradient and the osmoreceptors shrink.

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8
Q

What is the signifcance of the osmoreceptor shrinking?

A

The shrinking increases osmoreceptor firing.

Vasopressin is released from hypothalamic paraventricular nucleus and the supraoptic nucleus. Nuclei are groups of neuronal cell bodies.

Plasma osmolality is restored.

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9
Q

What is diabetes insipidus?

A

Absence or lack of circulating vasopressin. You cannot reabsorb water from the collecting duct

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10
Q

What are the 2 types of diabetes insipidus?

A
  1. Cranial
  2. Nephrogenic (end organ resistance to vasopressin)
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11
Q

Describe cranial (acquired) diabetes insipidus

A

Occurs due to damage of the hypophysial system.

Reasons for this happening include:

  • Traumatic brain injury
  • Pituitary surgery
  • Pituitary tumours, craniopharyngioma (brain tumour derived from pituitary tissue)
  • Metastasis to the pituitary glad (e.g. from breast)
  • Granulomatous infiltration of median eminence e.g. TB, sarcoidosis- stalk issues issues between the communication of the hypothalamus and the PPG.
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12
Q

Congenital cranial diabetes insipidus

A

RARE

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13
Q

Congential nephrogenic diabetes insipidus

A

If it does occur, it is due to a mutation in the gene coding for any of the receptors/ proteins in the aquaporin pathway (e.g. in the V2 receptors)

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14
Q

Acquired nephrogenic diabetes insipidus

A

Due to drugs (like lithium)

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15
Q

General signs and symptoms of diabetes insipidus

A
  • Large volumes of urine (polyuria)
  • Dilute urine (hypo-osmolar)
  • Thirst and increased drinking (polydipsia)
  • Dehydration (and consequences) if fluid intake is not maintained it can lead to death
  • Disruption during sleep with these problems
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16
Q

What is psychogenic polydipsia?

A

Patients present with the same symptoms as someone with DI.

Seen in psychiatric patients- may reflect anti-cholinergic effects of medication (dry mouth).

Also seen in patients who are told to drink a lot of fluids.

They may have Excess fluid intake (polydipsia) and excess urine output (polyuria) but they still have the ability to secrete vasopressin in response to osmotic stimuli is preserved.